Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
There is a negative correlation of testosterone levels with plasminogen activator inhibitor-1 (PAI-1) (Glueck et al 1993; Phillips 1993), which is a major prothrombotic factor and known to be associated with progression of atherosclerosis, as well as other prothrombotic factors fibrinogen, α2-antiplasmin and factor VII (Bonithon-Kopp et al 1988; Glueck et al 1993; Phillips 1993; De Pergola et al 1997). There is a positive correlation with tissue plasminogen activator (tPA) which is one of the major fibrinolytic agents (Glueck et al 1993). Interventional trials have shown a neutral effect of physiological testosterone replacement on the major clotting factors (Smith et al 2005) but supraphysiological androgen administration can produce a temporary mild pro-coagulant effect (Anderson et al 1995).

Cross-sectional studies have found a positive association between serum testosterone and some measures of cognitive ability in men (Barrett-Connor, Goodman-Gruen et al 1999; Yaffe et al 2002). Longitudinal studies have found that free testosterone levels correlate positively with future cognitive abilities and reduced rate of cognitive decline (Moffat et al 2002) and that, compared with controls, testosterone levels are reduced in men with Alzheimer’s disease at least 10 years prior to diagnosis (Moffat et al 2004). Studies of the effects of induced androgen deficiency in patients with prostate cancer have shown that profoundly lowering testosterone leads to worsening cognitive functions (Almeida et al 2004; Salminen et al 2004) and increased levels of serum amyloid (Gandy et al 2001; Almeida et al 2004), which is central to the pathogenesis of Alzheimer’s disease (Parihar and Hemnani 2004). Furthermore, testosterone reduces amyloid-induced hippocampal neurotoxity in vitro (Pike 2001) as well as exhibiting other neuroprotective effects (Pouliot et al 1996). The epidemiological and experimental data propose a potential role of testosterone in protecting cognitive function and preventing Alzheimer’s disease.
Also, due to the intake of these synthetic substances, men start behaving in a very excited way, as well as demonstrate high levels of aggression and even violence. So, the men’s behavior may be antisocial. In addition, the men will experience breast enlargement and testicular shrinkage. The other adverse effects include hypertension, tumor growth, heart attacks and strokes, as well as development of liver disorders. It’s obvious that the numerous dangers of steroid use far outweigh a few benefits which they bring.
That testosterone decreases with age has been clearly established by many studies over many years in several different populations of men (Harman et al 2001; Feldman et al 2002; Araujo et al 2004; Kaufman and Vermeulen 2005). Of even greater significance is the steeper fall of the most biologically active fraction of total testosterone, non-sex hormone binding globulin (SHBG)- bound testosterone, or bioavailable testosterone (bio-T). The classical, but not the only approach to measuring bio-T, is to precipitate out SHBG (and hence the testosterone which is strongly bound to it as well) and measure the remainder as total testosterone (Tremblay 2003). Vermeulen et al (1999) have devised a less tedious and less expensive method of measuring a surrogate for bio-T, namely calculated bio-T, inserting total T, albumin, SHBG and a constant into a mathematical formulation. There is a strong correlation between actual bio-T and calculated bio-T (Emadi-Konjin et al 2003).
Epidemiological studies have also assessed links between serum testosterone and non-coronary atherosclerosis. A study of over 1000 people aged 55 years and over found an inverse correlation between serum total and bioavailable testosterone and the amount of aortic atherosclerosis in men, as assessed by radiological methods (Hak et al 2002). Increased intima-media thickness (IMT) is an early sign of atherosclerosis and has also been shown to predict cardiovascular mortality (Murakami et al 2005). Cross-sectional studies have found that testosterone levels are negatively correlated with carotid IMT in independently living men aged 74–93 years (van den Beld et al 2003), diabetic men (Fukui et al 2003) and young obese men (De Pergola et al 2003). A 4-year follow up study of the latter population showed that free testosterone was also inversely correlated with the rate of increase of IMT (Muller et al 2004).

Epidemiological evidence supports a link between testosterone and glucose metabolism. Studies in non-diabetic men have found an inverse correlation of total or free testosterone with glucose and insulin levels (Simon et al 1992; Haffner et al 1994) and studies show lower testosterone levels in patients with the metabolic syndrome (Laaksonen et al 2003; Muller et al 2005; Kupelian et al 2006) or diabetes (Barrett-Connor 1992; Andersson et al 1994; Rhoden et al 2005). A study of patients with type 2 diabetes using measurement of serum free testosterone by the gold standard method of equilibrium dialysis, found a 33% prevalence of biochemical hypogonadism (Dhindsa et al 2004). The Barnsley study demonstrated a high prevalence of clinical and biochemical hypogonadism with 19% having total testosterone levels below 8 nmol/l and a further 25% between 8–12 nmol/l (Kapoor, Aldred et al 2007). There are also a number longitudinal studies linking low serum testosterone levels to the future development of the metabolic syndrome (Laaksonen et al 2004) or type 2 diabetes (Haffner et al 1996; Tibblin et al 1996; Stellato et al 2000; Oh et al 2002; Laaksonen et al 2004), indicating a possible role of hypogonadism in the pathogenesis of type 2 diabetes in men. Alternatively, it has been postulated that obesity may be the common link between low testosterone levels and insulin resistance, diabetes and cardiovascular disease (Phillips et al 2003; Kapoor et al 2005). With regard to this hypothesis, study findings vary as to whether the association of testosterone with diabetes occurs independently of obesity (Haffner et al 1996; Laaksonen et al 2003; Rhoden et al 2005).
Vitamin D, a steroid hormone, is essential for the healthy development of the nucleus of the sperm cell, and helps maintain semen quality and sperm count. Vitamin D also increases levels of testosterone, which may boost libido. In one study, overweight men who were given vitamin D supplements had a significant increase in testosterone levels after one year.5
As you cut these dietary troublemakers from your meals, you need to replace them with healthy substitutes like vegetables and healthy fats (including natural saturated fats!). Your body prefers the carbohydrates in micronutrient-dense vegetables rather than grains and sugars because it slows the conversion to simple sugars like glucose, and decreases your insulin level. When you cut grains and sugar from your meals, you typically will need to radically increase the amount of vegetables you eat, as well as make sure you are also consuming protein and healthy fats regularly.

A team led by Dr. Joel Finkelstein at Massachusetts General Hospital investigated testosterone and estradiol levels in 400 healthy men, 20 to 50 years of age. To control hormone levels, the researchers first gave the participants injections of a drug that suppressed their normal testosterone and estradiol production. The men were randomly assigned to 5 groups that received different amounts (from 0 to 10 grams) of a topical 1% testosterone gel daily for 16 weeks. Half of the participants were also given a drug to block testosterone from being converted to estradiol.
We all remember the time during our teens where our body underwent majority of its changes that led us into adulthood. As far as testosterone levels go, this period of time is where the production of this hormone peaked. Testosterone levels during these teenage years remain high and consistent, and therefore it is not advisable to use a testosterone boosting supplement during this time. This is because, Natural Testosterone Boosters work by encouraging your body to increase it;s natural levels back to their maximum capacity. If your body is already producing it’s maximum amount of Testosterone, these products will be ineffective for you. You should be prioritising quality, intense training sessions with adequate nutrition, rich in protein and carbohydrates to elicit growth and repair.

The natural production of DHEA is also age-dependent. Prior to puberty, the body produces very little DHEA. Production of this prohormone peaks during your late 20’s or early 30’s. With age, DHEA production begins to decline. The adrenal glands also manufacture the stress hormone cortisol, which is in direct competition with DHEA for production because they use the same hormonal substrate known as pregnenolone. Chronic stress basically causes excessive cortisol levels and impairs DHEA production, which is why stress is another factor for low testosterone levels.
Researchers found that the simple act ‘expressing power through open, expansive postures’ (i.e. standing up straight and proud) can increase Testosterone and decrease cortisol (58), along with improving feelings of power and tolerance for risk. Easy! Your mother was right – don’t slouch. This could be a handy trick before making a speech or going on a date!

Vitamin D, a steroid hormone, is essential for the healthy development of the nucleus of the sperm cell, and helps maintain semen quality and sperm count. Vitamin D also increases levels of testosterone, which may boost libido. In one study, overweight men who were given vitamin D supplements had a significant increase in testosterone levels after one year.5
Remember that each person is unique, and each body responds differently to treatment. TT may help erectile function, low sex drive, bone marrow density, anemia, lean body mass, and/or symptoms of depression. However, there is no strong evidence that TT will help memory recall, measures of diabetes, energy, tiredness, lipid profiles, or quality of life.
How do you boost testosterone naturally? Testosterone is a male sex hormone. Low levels can cause changes to the distribution of body fat and muscle strength. Testosterone reduces with age, but people can boost it with lifestyle changes, including diet and exercise. Adequate sleep, nutritional supplements, and stress reduction may also help. Learn more here. Read now
Exercise boosts testosterone in two important ways. First, specific types of exercise actually cause our body to produce more testosterone. We’ll talk more about those in a bit. Second, exercise helps to increase muscle mass and decrease body fat. As we’ve discussed previously, adipose tissue converts testosterone into estrogen. The less fat we get, the more T we have.
As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone. 
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A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).


In general, the normal range in males is about 270 to 1070 ng/dL with an average level of 679 ng/dL. A normal male testosterone level peaks at about age 20, and then it slowly declines. Testosterone levels above or below the normal range are considered by many to be out of balance. Moreover, some researchers suggest that the healthiest men have testosterone levels between 400 - 600 ng/dL.
Men on long-term testosterone appear to have a higher risk of cardiovascular problems, like heart attacks, strokes, and deaths from heart disease. For example, in 2010, researchers halted the Testosterone in Older Men study when early results showed that men on hormone treatments had noticeably more heart problems. "In older men, theoretical cardiac side effects become a little more immediate," Dr. Pallais says.
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